Anaesthesia for NEET PG 2026: High-Yield Topics, Spinal Complications, and Drug Doses

Anaesthesia contributes approximately 2–3% of the NEET PG paper — around 3 to 6 questions out of 180. That is a narrow target. The good news is that Anaesthesia has one of the highest PYQ repetition rates of any subject in NEET PG. The same topics appear, in the same formats, cycle after cycle. If you know the right 15 to 20 concepts well, you can reliably get every Anaesthesia question correct.

This guide covers every high-yield Anaesthesia topic with the level of detail NEET PG actually tests. Not a textbook summary — a focused, exam-relevant breakdown of what appears in PYQs and why. For where this subject sits against the rest of the paper, see our subject wise weightage guide; for how to fit it into your overall approach, see the complete NEET PG preparation strategy.

Why Anaesthesia Is Easier Than It Looks

Most aspirants either over-prepare Anaesthesia — spending weeks on a subject worth 2–3% of the paper — or under-prepare it, avoiding it entirely and dropping guaranteed marks. The correct approach is systematic PYQ-based preparation of the 15 core topics listed below, spending approximately 5 to 7 focused study days on the entire subject.

Anaesthesia questions in NEET PG are almost never about clinical judgment — they are about pharmacological facts, mechanism comparisons, and specific clinical scenarios that have a single correct answer. Pattern recognition after PYQ practice is highly reliable here.

Before diving into topics, use the NEET PG 2026 score calculator to understand how much these 3 to 6 questions are actually worth to your rank. Getting all Anaesthesia questions correct versus none is a score swing of 12 to 24 marks — potentially 1,000 or more rank positions in the competitive range.

The 15 Most-Tested Anaesthesia Topics in NEET PG PYQs

Based on analysis of 14 years of NEET PG papers:

Rank	Topic	Frequency	Format
1	Malignant hyperthermia — triggers, mechanism, treatment	Very High	Clinical scenario MCQ
2	Spinal anaesthesia — layers pierced, drugs, complications	Very High	Direct factual + clinical
3	Local anaesthetic — classification, mechanism, max doses	Very High	Pharmacology MCQ
4	NMS vs malignant hyperthermia — comparison	High	Differentiation MCQ
5	Stages of general anaesthesia (Guedel's)	High	Direct factual
6	MAC values of inhalational agents	High	Comparison MCQ
7	Adrenaline in local anaesthetics — reasons and exceptions	High	Pharmacology reasoning
8	Muscle relaxants — depolarising vs non-depolarising	High	Classification MCQ
9	Suxamethonium — mechanism, adverse effects, contraindications	High	Pharmacology MCQ
10	Epidural anaesthesia — indications, technique, differences from spinal	Moderate	Procedural MCQ
11	Neuroleptic malignant syndrome	Moderate	Clinical scenario
12	Bupivacaine cardiotoxicity	Moderate	Direct factual
13	Ketamine — unique properties and uses	Moderate	Pharmacology MCQ
14	Propofol — uses, PRIS, contraindications	Moderate	Clinical MCQ
15	Pre-medication drugs and their rationale	Low-Moderate	Pharmacology MCQ

Topic 1: Spinal Anaesthesia

Layers Pierced (skin to subarachnoid space)

This is the single most-tested anatomical fact in Anaesthesia. Seven layers are pierced when performing a spinal anaesthetic:

1. Skin
2. Subcutaneous tissue
3. Supraspinous ligament
4. Interspinous ligament
5. Ligamentum flavum
6. Epidural space (and epidural fat / venous plexus)
7. Dura mater and arachnoid mater (often counted together in exam questions)

Memory aid: "Silly Surgeons in Labs Eat Dead Animals" — Skin, Subcutaneous tissue, Interspinous ligament, Ligamentum flavum, Epidural space, Dura mater, Arachnoid mater.

PYQ pattern: questions ask either for the complete list in order, or specifically which ligament is felt as a sudden loss of resistance — the ligamentum flavum.

Level of Spinal Anaesthesia

Spinal is performed between L3–L4 or L4–L5 in adults, below the conus medullaris, which ends at L1–L2 in adults. In children the spinal cord extends to L2–L3, so spinal is performed at L4–L5.

Drugs Used in Spinal Anaesthesia

Drug	Type	Onset	Duration	Key Use
Bupivacaine 0.5% heavy	Hyperbaric LA	Slow	Long (2–4 hrs)	Most common agent
Lignocaine (hyperbaric)	LA	Fast	Short (1–2 hrs)	Short procedures
Fentanyl	Opioid adjuvant	Fast	Adds 2–4 hrs	Combined with LA
Morphine	Opioid adjuvant	Slow	12–24 hrs	Post-op analgesia
Clonidine	Alpha-2 agonist	—	Extends duration	Adjuvant

A "heavy" or hyperbaric solution has a higher specific gravity than CSF, so it sinks with gravity and its spread is position-dependent.

Complications of Spinal Anaesthesia

This is the highest-yield topic area for clinical scenario questions.

Immediate complications:

Complication	Mechanism	Management
Hypotension	Sympathetic block causing vasodilation	IV fluids, vasopressors (ephedrine first-line), left lateral tilt in pregnancy
Bradycardia	Block of cardiac accelerator fibres (T1–T4)	Atropine, ephedrine
High or total spinal	Drug spreads to brainstem	Immediate intubation, vasopressors, CPR if needed
Urinary retention	Sacral parasympathetic block	Catheterisation
Nausea and vomiting	Hypotension plus vagal response	Treat the hypotension first

Delayed complications:

Complication	Onset	Features	Management
Post-dural puncture headache (PDPH)	24–48 hours	Positional — worse sitting or standing, better lying flat; frontal or occipital	Bed rest, hydration, caffeine; epidural blood patch if persistent
Neurological complications	Variable	Transient neurological symptoms, cauda equina syndrome	Rare; supportive
Meningitis	Days	Bacterial or chemical	Antibiotics
Backache	Days	Common, usually resolves	Conservative

PDPH is a PYQ favourite. The positional nature — relieved by lying flat — is the diagnostic key. It occurs because of persistent CSF leak through the dural hole, causing traction on the meninges when upright.

Factors that make PDPH more likely:

• Larger needle size
• Cutting (Quincke) needles rather than pencil-point (Whitacre, Sprotte) needles
• Younger patients and females
• Multiple attempts

Spinal anaesthesia recovery time: motor block resolves before sensory block. Sensory block at the surgical site resolves in 1.5 to 3 hours for most agents. Full sensory and motor recovery occurs within 2 to 4 hours for a standard bupivacaine spinal. Urinary function usually takes longest to return, at 2 to 6 hours, which is why catheterisation may be needed for longer procedures.

Topic 2: Local Anaesthetics

Classification

Esters, metabolised by plasma cholinesterase:

• Cocaine — the only vasoconstricting LA, because it inhibits noradrenaline reuptake
• Procaine
• Chloroprocaine — shortest duration, fastest hydrolysis
• Tetracaine / amethocaine — topical and spinal use
• Benzocaine — topical only

Amides, metabolised by hepatic enzymes and therefore slower:

• Lignocaine / lidocaine — the most versatile; LA and antiarrhythmic
• Bupivacaine — longest duration, most cardiotoxic
• Ropivacaine — less cardiotoxic than bupivacaine, preferred in obstetrics
• Levobupivacaine — S-enantiomer of bupivacaine, less cardiotoxic
• Prilocaine — causes methaemoglobinaemia
• Mepivacaine

Memory aid: amides have an extra "i" in the name — bupivAcaIne, lIgnocaIne, ropIvacaIne.

Mechanism of Action

Local anaesthetics block sodium channels from inside the channel, binding preferentially to the inactivated state and only once the channel has opened. They are weak bases with a pKa above 7.4. The unionised form crosses the nerve membrane; the ionised form, once inside the cell, blocks the channel.

This is why local anaesthetic works poorly in inflamed or infected tissue: the acidic pH leaves more drug in the ionised form outside the cell, so less crosses the membrane.

Order of Nerve Blockade

The smallest-diameter and unmyelinated fibres are blocked first: pain (C fibres), then temperature, then touch, then pressure, and motor last.

NEET PG key point: autonomic (sympathetic) block occurs first, which is why hypotension appears before the surgical site is anaesthetised. Motor function recovers last.

Maximum Safe Doses

This is tested directly, usually in clinical scenario format.

Agent	Without Adrenaline	With Adrenaline	Key Notes
Lignocaine	3 mg/kg	7 mg/kg	Standard LA; also antiarrhythmic
Bupivacaine	2 mg/kg	2.5 mg/kg	Most cardiotoxic; adrenaline adds little
Ropivacaine	3 mg/kg	4 mg/kg	Less cardiotoxic than bupivacaine
Prilocaine	6 mg/kg	8.5 mg/kg	Highest plain dose; methaemoglobinaemia risk
Cocaine	1.5–3 mg/kg	Not added — already vasoconstricts	Only intrinsically vasoconstrictive LA

Worked calculation, the format PYQs use: a patient weighs 70 kg. Maximum safe dose of plain lignocaine is 3 mg/kg, so 210 mg. Lignocaine 2% is 20 mg/mL. Maximum volume is 210 ÷ 20 = 10.5 mL.

Why Adrenaline Is Added

Adrenaline is added to local anaesthetics to cause local vasoconstriction, which reduces systemic absorption, lowers the peak plasma concentration and therefore the toxicity risk. It also prolongs the duration of action — especially for shorter-acting agents like lignocaine — reduces bleeding in the surgical field, and acts as a marker of accidental intravascular injection, producing tachycardia.

Where adrenaline must not be added:

• Ring blocks of digits, penis or pinna — end arteries, with risk of ischaemia and gangrene
• Intravenous regional anaesthesia (Bier's block) — systemic release when the tourniquet is deflated
• Patients on MAO inhibitors or tricyclics — hypertensive crisis
• Patients with severe hypertension or cardiac arrhythmias

Topic 3: Malignant Hyperthermia

Malignant hyperthermia is a pharmacogenetic disorder of skeletal muscle characterised by uncontrolled calcium release from the sarcoplasmic reticulum following exposure to a triggering agent. It is an emergency with high mortality if untreated.

Genetic basis: mutation in the ryanodine receptor gene (RYR1) on chromosome 19q13, inherited in an autosomal dominant pattern.

Triggering Agents

Remember the triggers as "SHE": Suxamethonium (succinylcholine), Halogenated inhalational agents (halothane, sevoflurane, desflurane, isoflurane, enflurane), and Exercise and heat in susceptible individuals.

Safe in MH-susceptible patients: all intravenous agents (propofol, ketamine, thiopentone), all non-depolarising muscle relaxants (vecuronium, rocuronium, atracurium), all local anaesthetics, and nitrous oxide.

Clinical Features

Feature	Explanation
Hypercapnia (rising EtCO2)	Earliest and most sensitive sign — increased metabolism
Tachycardia	Earliest cardiovascular sign
Masseter muscle spasm	Jaw rigidity after suxamethonium
Muscle rigidity	Generalised
Hyperthermia	Core temperature rising more than 2°C per hour — a late sign
Metabolic acidosis	Increased CO2 production and lactate accumulation
Rhabdomyolysis	Myoglobinaemia, myoglobinuria, dark urine
Hyperkalaemia	From muscle breakdown; can cause cardiac arrest

NEET PG key point: the earliest sign is a rise in end-tidal CO2, not hyperthermia — which is a late sign despite giving the condition its name.

Management

Stop, cool, dantrolene.

1. Stop all triggering agents immediately
2. Call for help — this is a team emergency
3. Switch to total intravenous anaesthesia with propofol
4. Hyperventilate with 100% oxygen at high flow, at least 10 L/min
5. Give dantrolene, the only specific antidote — 2.5 mg/kg IV bolus, repeated every 5 minutes up to 10 mg/kg total; it blocks the ryanodine receptor and stops calcium release from the sarcoplasmic reticulum. Continue oral dantrolene for 24–48 hours to prevent recurrence
6. Cool actively with cold IV saline, ice packs and cooling blankets
7. Treat hyperkalaemia with calcium gluconate, sodium bicarbonate and insulin-dextrose
8. Correct acidosis with sodium bicarbonate
9. Maintain urine output with fluids and furosemide to prevent myoglobin-induced acute kidney injury
10. Monitor for DIC, arrhythmias and renal failure

Topic 4: NMS vs Malignant Hyperthermia

This distinction appears in virtually every NEET PG cycle in some form. Know every row.

Feature	Malignant Hyperthermia	Neuroleptic Malignant Syndrome
Setting	During or shortly after general anaesthesia	Days to weeks after starting an antipsychotic
Triggers	Suxamethonium, halogenated volatile agents	Dopamine antagonists — haloperidol, chlorpromazine, metoclopramide, droperidol
Mechanism	Excess calcium release from SR via RYR1 mutation	Dopamine D2 receptor blockade in striatum and hypothalamus
Inheritance	Autosomal dominant (RYR1, chromosome 19)	Not inherited — idiosyncratic drug reaction
Onset	Minutes to hours	Hours to days
Muscle rigidity	Lead-pipe or cogwheel	Lead-pipe
Hyperthermia	Severe, may exceed 40–42°C	Severe, 38.5–40°C
Earliest sign	Rising EtCO2	Altered mental status and rigidity
Creatine kinase	Markedly elevated	Markedly elevated
Specific antidote	Dantrolene, 2.5 mg/kg IV	Bromocriptine, plus dantrolene
Other treatment	Stop volatile agent, TIVA, cooling, oxygen	Stop the antipsychotic, benzodiazepines
Diagnosis	Caffeine-halothane contracture test on muscle biopsy	Clinical — no specific test

Memory tip: in MH the drug *causes* muscle to release calcium. In NMS the drug *blocks* dopamine receptors in the striatum, producing rigidity. MH uses dantrolene alone; NMS uses bromocriptine to restore dopaminergic tone, plus dantrolene.

Topic 5: Stages of General Anaesthesia (Guedel's Classification)

Stage	Name	Clinical Features	Significance
1	Analgesia / induction	Conscious; analgesia without amnesia, then with amnesia; reflexes intact	Nitrous oxide works in Stage 1 only
2	Excitement / delirium	Unconscious but reflexes exaggerated; irregular breathing, breath-holding, vomiting, laryngospasm risk	The danger zone — avoid stimulation; pass through rapidly
3	Surgical anaesthesia	Regular breathing, loss of reflexes; divided into 4 planes	Target stage for surgery
4	Medullary depression	Respiration and vasomotor centre cease	Anaesthetic overdose — death

Planes within Stage 3:

Plane	Respiration	Eye Signs	Muscle Tone	Reflexes
1	Regular	Eyeball moves; lacrimation	Mild loss	Pharyngeal reflex lost
2	Regular	Eyeball fixed centrally	Moderate loss	Corneal reflex lost
3	Intercostal paralysis begins	Fixed, dilated pupil	More loss	Laryngeal reflex lost
4	Complete intercostal paralysis	Fixed, dilated pupil	Total flaccidity	All reflexes lost

PYQ pattern: questions ask what is lost at which plane, or which sign indicates overdose — fixed dilated pupils with cessation of respiration means Stage 4.

Topic 6: Inhalational Agents and MAC Values

MAC, the minimum alveolar concentration, is the alveolar concentration that prevents movement in 50% of patients in response to a standard surgical stimulus. Lower MAC means more potent.

Agent	MAC (%)	Properties
Halothane	0.75	Most potent traditional agent; hepatotoxic; sensitises heart to catecholamines; MH trigger
Isoflurane	1.15	Preferred for neuroanaesthesia; coronary steal; pungent, so poor for induction
Sevoflurane	2.0	Best for inhalational induction, least pungent; paediatric use; produces Compound A with soda lime at low flow
Desflurane	6.0	Highest MAC, least potent; fastest recovery; very pungent, cannot be used for induction
Nitrous oxide	105	MAC above 100% means it cannot produce surgical anaesthesia alone; adjuvant only; supports combustion

PYQ patterns: best for inhalational induction in children is sevoflurane; most potent is halothane; fastest recovery is desflurane; cannot produce surgical anaesthesia alone is nitrous oxide; causes coronary steal is isoflurane.

Topic 7: Muscle Relaxants

Feature	Depolarising (suxamethonium)	Non-depolarising
Mechanism	Mimics ACh at the NMJ, causing sustained depolarisation	Competitive antagonism of ACh at the NMJ
Fasciculations	Yes — characteristic	No
Train of four	No fade	Fade
Tetanic stimulation	No fade	Fade
Post-tetanic facilitation	Absent	Present
Reversal	Cannot be reversed pharmacologically	Neostigmine, or sugammadex for rocuronium and vecuronium
MH trigger	Yes	No

Suxamethonium

Fastest onset of any muscle relaxant at 30–60 seconds and the shortest duration at 5–10 minutes, which makes it the drug of choice for rapid sequence intubation. It is metabolised by plasma cholinesterase.

Adverse effects, all of them examined:

Adverse Effect	Mechanism
Hyperkalaemia	Potassium efflux during depolarisation — normally a 0.5 mEq/L rise, dangerous in burns, crush injury and denervation
Bradycardia	Muscarinic effect, especially with repeat doses
Raised intraocular pressure	Contraction of extraocular muscles
Raised intragastric pressure	Aspiration risk
Malignant hyperthermia	Trigger
Suxamethonium apnoea	Pseudocholinesterase deficiency
Myalgia	Post-operative muscle pain from fasciculations

Contraindications: burns after the first 48 hours and up to two years; crush injuries; spinal cord injury and upper motor neurone lesions; denervation injuries; MH susceptibility; pseudocholinesterase deficiency; open eye injuries.

Non-Depolarising Agents

Drug	Duration	Reversal	Key Feature
Rocuronium	Intermediate	Sugammadex or neostigmine	Fastest-onset non-depolariser; RSI alternative when suxamethonium is contraindicated
Vecuronium	Intermediate	Neostigmine	Least cardiovascular effect
Atracurium	Intermediate	Neostigmine	Hofmann elimination — safe in hepatic and renal failure
Cisatracurium	Intermediate	Neostigmine	Purified isomer of atracurium; less histamine release
Pancuronium	Long	Neostigmine	Vagolytic — causes tachycardia
Mivacurium	Short	Plasma cholinesterase	Shortest non-depolariser

Topic 8: Ketamine

Ketamine is the most pharmacologically distinctive general anaesthetic and carries its own set of NEET PG questions. It is an NMDA receptor antagonist producing dissociative anaesthesia — a dissociation between the thalamo-neocortical and limbic systems.

Property	Details
Cardiovascular	Stimulates the cardiovascular system — raises BP, heart rate and cardiac output; useful in shocked patients
Airway	Bronchodilator; safe in asthmatics
ICP and IOP	Raises both — contraindicated in head injury and open eye injury
Analgesia	Profound, even at sub-anaesthetic doses
Consciousness	Apparent wakefulness while disconnected from the environment
Emergence	Emergence delirium with hallucinations — prevented by benzodiazepine premedication
Muscle tone	Maintained or increased, unlike other agents
Secretions	Increased — premedicate with glycopyrrolate or atropine

High-yield uses: haemodynamically compromised patients, battlefield anaesthesia, paediatric procedural sedation, asthmatics, and dissociative analgesia. Contraindications: hypertension, ischaemic heart disease, raised ICP, open eye injury, psychiatric disorders and eclampsia.

Topic 9: Propofol

Feature	Detail
Formulation	White emulsion of egg lecithin and soybean oil
Mechanism	GABA-A receptor agonist
Onset and offset	Rapid — ideal for TIVA and day-case surgery
Cardiovascular	Drops blood pressure significantly through vasodilation and mild negative inotropy
Antiemetic	Intrinsically antiemetic — useful where PONV is a concern
Analgesia	None
Pain on injection	Common — mix with lignocaine or use a large vein
Propofol infusion syndrome	High-dose prolonged infusion causing metabolic acidosis, rhabdomyolysis, cardiac and renal failure; seen in the critically ill
Contraindications	Soy or egg allergy (relative); mitochondrial disease

High-Yield Anaesthesia PYQ Checklist

Use this as your revision list. Every item has appeared in NEET PG PYQs. Work through it alongside the NEET PG 3-month study plan if you are in the final stretch.

• Layers pierced in spinal anaesthesia, in order
• Earliest sign of malignant hyperthermia — rising EtCO2
• Specific antidote for MH and its dose — dantrolene 2.5 mg/kg
• NMS vs MH — triggers, mechanism, treatment
• Maximum safe dose of lignocaine without adrenaline — 3 mg/kg
• Maximum safe dose of lignocaine with adrenaline — 7 mg/kg
• Why adrenaline is not added in ring blocks
• The only vasoconstricting local anaesthetic — cocaine
• Local anaesthetics metabolised by plasma cholinesterase — the esters
• The LA causing methaemoglobinaemia — prilocaine
• The most cardiotoxic LA — bupivacaine
• MAC values: lowest is halothane, highest is nitrous oxide
• Best agent for inhalational induction — sevoflurane
• Guedel Stage 2 and why it is dangerous
• Sign of anaesthetic overdose — fixed dilated pupils with respiratory arrest
• Suxamethonium contraindications — burns, crush injury, MH susceptibility
• Cause of suxamethonium apnoea — pseudocholinesterase deficiency
• The drug undergoing Hofmann elimination — atracurium, safe in liver and kidney failure
• Fastest non-depolarising relaxant for RSI — rocuronium, reversed with sugammadex
• Ketamine raises ICP and IOP — contraindicated in head injury and open eye injury
• Ketamine as a cardiovascular stimulant — use in shocked patients
• Propofol infusion syndrome — features and risk factors
• Post-dural puncture headache — positional, treated with an epidural blood patch